The gut/brain access has a significant role in disease progression in Parkinson’s disease. There are several hypotheses for what is causing the progression itself; one of which is that the microbiome in the GI is creating SCFAs that are able to increase inflammation, a-synuclein originates in the GI and is able to travel to the brain causing a-synuclein aggregation and inflammation, and that the overall inflammation in the brain is causing activation of microglia causing increased a-synuclein aggregation. It is unknown which of these is causing the disease, but they all have been shown to have a role. It is known that a-synuclein aggregates cause motor symptoms and there is evidence to show that it originates from the dysbiosis of the GI microbiota. a-synuclein in the CNS activates microglia cells, increasing proinflammatory cytokines TNF-a and IL-6. The short chain fatty acids produced by fermentation byproducts of the gut microbiome play a role on the enteric nervous system and can be a major player of the nonmotor symptoms displayed by Parkinson’s disease patients and increasing inflammation. Lastly, the microbiome of Parkinson’s disease patients is altered from a normal gut microbiome to a disease-causing form. All of these factors play a role in Parkinson’s disease progression but the main treatment (L-DOPA) does not directly impact any of these factors.